HYPOXIA-INDUCIBLE FACTOR-1 ALPHA AND VASCULAR ENDOTHELIAL GROWTH FACTOR IN THE CAROTID ATHEROMA ARE EXPRESSED MORE IN SYMPTOMATIC CASES THAN IN ASYMPTOMATIC CASES

  • 大沢 知士
    Departments of Neurosurgery, Nagoya City University Medical School
  • 間瀬 光人
    Departments of Neurosurgery, Nagoya City University Medical School
  • 谷川 元紀
    Departments of Neurosurgery, Nagoya City University Medical School
  • 藤田 政隆
    Departments of Neurophysiology, Nagoya City University Medical School
  • 片野 広之
    Departments of Neurosurgery, Nagoya City University Medical School
  • 青山 公紀
    Departments of Neurosurgery, Nagoya City University Medical School
  • 大野 貴之
    Departments of Neurosurgery, Nagoya City University Medical School
  • 櫻井 圭太
    Departments of Radiology, Nagoya City University Medical School
  • 佐々木 繁
    Departments of Radiology, Nagoya City University Medical School
  • 山田 和雄
    Departments of Neurosurgery, Nagoya City University Medical School

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Objects: We studied the expression of hypoxia-inducible factor-1 alpha (HIF1-alpha) and vascular endothelial growth factor (VEGF) in the carotid plaques, because they are involved in the tissue neovascularization and the resulting symptomatic transformation of asymptomatic carotid stenosis. We also explored the relation of tissue expression of HIF1-alpha and VEGH to preoperative MRI plaque imaging. Methods: We undertook immunohistochemical staining of endarterectomy tissues of 13 patients for HIF1-alpha and VEGF. We also undertook double immunostaining for macrophages of smooth muscle cells and HIF1-alpha or VEGF in order to identify the source cells of HIF1-alpha and VEGF. Immunostaining results and histological grading of atherosclerosis as defined by American Heart Association (AHA) were compared to preoperative profiles of the patients including plaque imaging on MRI. Results: Both HIF1-alpha and VEGF were expressed in the carotid plaques and the sources of those hypoxia-related proteins were macrophages and smooth muscle cells. Plaques from symptomatic patients expressed HIF1-alpha and VEGF more strongly than those from asymptomatic patients. The degree of carotid stenosis and plaque intensity on MRI had no correlation with the plaques obtained from the symptomatic or asymptomatic group. However, high-intensity carotid plaques had a significantly more advanced histological grading of atherosclerosis as defined by AHA. Conclusion: Symptomatic carotid plaques express more HIF1-alpha and VEGF. This may have a role in neovascularization and plaque hemorrhage, causing symptomatic transformation of asymptomatic plaques.

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